Zahra Rahimi , Mansour Salehi , Abbas Dousti ,
Volume 11, Issue 3 (5-2017)
Abstract
ABSTRACT
Background and objective: Approximately 50 million people worldwide (1% of the world's population) suffer from epilepsy. Among 700 thousand people with epilepsy in Iran, 20% have refractory epilepsy. Accumulation of leukocytes in patients' brain parenchyma is thought to be related to different types of epilepsy. Recent clinical observations suggest that therapeutic strategies that interfere with leukocytes or cause them to migrate may have therapeutic efficacy in epilepsy. The aim of this study was to identify treatment-resistant patients, and investigate the association between polymorphism rs1024611 in CCL2 gene and drug resistance in patients with epilepsy in Isfahan, Iran.
Methods: Blood samples were taken from 50 patients with intractable epilepsy (case group) and 50 drug-responsive patients with epilepsy (control group). Genomic DNA was extracted from peripheral blood by salting out method. Specific primers were designed by Oligo 7 software to investigate polymorphism rs1024611 using PCR-RFLP. The preliminary results for a number of samples were confirmed by sequencing.
Results: The results of this study showed that there was a significant relationship between intractable epilepsy and presence of C allele.
Conclusion: Similar to previous study, we found a significant association between CCL2 gene polymorphism and drug-resistant epilepsy.
Keywords: Epilepsy, Drug Resistance, Polymorphism, CCL2.
Bahar Yazdani, Hussein Anani, Iman Baluchi, Behjat Kalantary Khandany, Gholamhossein Hassanshahi,
Volume 15, Issue 4 (7-2021)
Abstract
Background and objectives: Acute myeloid leukemia (AML) is a malignancy that involves the bone marrow and peripheral blood. Some chemokines play a role in the progression, migration and tumor initiation and are therefore associated with poor prognosis. CCL2 promotes tumor growth and is associated with poor prognosis in AML patients. We investigated effects of chemotherapy on serum level of CCL2 in AML patients.
Methods: Throughout this case-control study, blood samples were collected from 25 healthy individuals and 25 AML (M4 and M5) patients before and after the first stage of the current chemotherapy regimen (7+3). Serum level of CCL2 was measured using commercial ELISA kits. Data were analyzed in SPSS 22 using the two-sample t-test and paired t-test.
Results: Before chemotherapy, serum level of CCL2 was significantly higher in the patients than in the healthy controls. Following chemotherapy, the serum level of CCL2 reduced significantly to a level comparable to that of the healthy controls.
Conclusion: The current chemotherapy (7+3) can effectively inhibit CCL2 in AML patients.
